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This evidence was strengthened by studies in vivo in which manipulation of calpastatin levels, an endogenous calpain inhibitor, led to modulation of the neurological phenotype seen in a SCA3 mouse model, as well as of mutant ATXN3 aggregation and neurodegeneration, consistent with a role for calpain activation in pathogenesis [50, 52]

doi: 10.1084/JEM.20080091 101 PeisleyALinCWuBOrme-JohnsonMLiuMWalzTet al

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